The results reported here suggest that small craniotomy evacuation with a flexible endoscope is a safe, effective, and minimally invasive treatment for acute and subacute SDH in selected cases.

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OBJECTIVE Shunt-dependent hydrocephalus (SDHC) may arise after aneurysmal subarachnoid hemorrhage (aSAH) as CSF resorptive mechanisms are disrupted. Using propensity score analysis, the authors aimed to investigate which treatment modality, surgical clipping or endovascular treatment, is superior in reducing rates of SDHC after aSAH. METHODS The authors' multicenter SAH database, comprising 3 stroke centers affiliated with Kyoto University, Japan, was used to identify patients treated between January 2009 and July 2016. Univariate and multivariate analyses were performed to characterize risk factors for SDHC after aSAH. A propensity score model was generated for both treatment groups, incorporating relevant patient covariates to detect any superiority for prevention of SDHC after aSAH. RESULTS A total of 566 patients were enrolled in this study. SDHC developed in 127 patients (22%). On multivariate analysis, age older than 53 years, the presence of intraventricular hematoma, and surgical clipping as opposed to endovascular coiling were independently associated with SDHC after aSAH. After propensity score matching, 136 patients treated with surgical clipping and 136 with endovascular treatment were matched. Propensity score-matched cohorts exhibited a significantly lower incidence of SDHC after endovascular treatment than after surgical clipping (16% vs 30%, p = 0.009; OR 2.2, 95% CI 1.2-4.2). SDHC was independently associated with poor neurological outcomes (modified Rankin Scale score 3-6) at discharge (OR 4.3, 95% CI 2.6-7.3; p < 0.001). CONCLUSIONS SDHC after aSAH occurred significantly more frequently in patients who underwent surgical clipping. Strategies for treatment of ruptured aneurysms should be used to mitigate SDHC and minimize poor outcomes.

Objective: Contrast agent neurotoxicity is a rare complication of neurovascular intervention. Here we report two cases of symptomatic contrast-induced encephalopathy after coil embolization for unruptured cerebral aneurysms. Case presentation: A 75-year-old man with right unruptured anterior cerebral artery aneurysm and a 65-year-old woman with left unruptured internal carotid artery aneurysm underwent endovascular coil embolization. Immediately after the procedure, the male patient showed left hemiparesis, and the female patient showed right hemiparesis and aphasia. Non-contrast computed tomography (CT) showed cortical enhancement in the affected cerebral hemisphere immediately after the procedure and complete resolution of the abnormal findings the next day. Magnetic resonance imaging revealed a few small infarctions that were not considered responsible for the neurological symptoms. Clinical symptoms resolved completely within 3 days after procedures using only conservative therapy. Therefore, both patients were diagnosed with contrast-induced encephalopathy. Conclusion: Although the precise mechanisms underlying contrast-induced encephalopathy remain unclear, one possible reason for this complication is osmotic disruption of the blood-brain barrier. Endovascular neurosurgeons should be aware of this rare complication during and after endovascular treatment.

The induction of large-scale plasticity in the adult brain should be key for recovery from severe damage of the central nervous system. Here, drastic motor recovery was observed after subhemisection spinal cord injury in macaques that received intensive training and cortical electrical stimulation. During recovery, movement-related activity increased in ipsilesional sensorimotor areas and functional connectivity from ipsilesional to contralesional areas was strengthened. Electrical stimulation applied widely across bilateral sensorimotor areas induced muscle twitches in affected and intact forelimbs. The interhemispheric inhibition observed before injury was switched to facilitation. Furthermore, massive re-routing occurred in corticospinal axons from the contralesional motor cortex. Such global disinhibition and massive plasticity would open the workspace for the reorganization of motor networks to recruit novel areas for recovery.